The vast majority of excitatory neurotransmission is mediated by AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors1. The functional receptor exists as a tetramer, either homomers or heteromers, from a repertoire of 4 different subunits, GluA1 – GluA41. It is well known that glutamate is a neurotoxin and it is proposed that overactivation of ionotropic glutamate receptors may underlie many neurodegenerative disorders such as ischemic stroke, epilepsy, Parkinson’s and dementia2. Enhancement of AMPA receptor activation by, for example, BDNF, has been proposed to have beneficial effects of learning and memory and has potential therapeutic value in the treatment of depression, Huntington’s and Parkinson’s diseases1. We have used GluA2 receptors expressed in HEK cells on 3 different automated patch clamp systems recording from either 1, 8 or 384 wells simultaneously. GluA2 was activated by glutamate, inhibited by CNQX and potentiated by LY404187.

In addition to GluA2 expressed in HEK cells, we also recorded glutamatergic-enriched cortical neurons derived from induced pluripotent stem cells on an automated patch clamp platform. In these neurons we recorded various voltage-gated channels. In addition, glutamate responses were recorded which were potentiated by LY404187.

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